Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors have found morphological alterations identical with hyperfiltration glomerular injury in the renal biopsies of 23 out of 100 patients with IgA nephropathy. In 15 of them the lesions were similar to the different stages of segmental glomerular hyalinosis and sclerosis with deposition of IgM and C3. At the time of renal biopsy, the serum creatinine of all except 8 patients was normal (maximally 170 mumol/1), only 13 had hypertension, and all except 2 were proteinuric. During the follow-up period (mean +/- 2Sd = 138 +/- 76 months) all of them became hypertensive. In 10 patients end-stage renal failure developed, and in another 10, serum creatinine also became elevated (range 124 - 504 mumol/1). On the basis of these data the development of focal segmental hyalinosis and sclerosis should be interpreted as a bad prognostic sign in IgA nephropathy.
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PMID:Hyperperfusion injury in IgA nephropathy. 184 35

The authors have found morphological alterations identical with hyperfiltration glomerular injury in the renal biopsies of 23 out of 100 patients with IgA nephropathy. In 15 of them the lesions were similar to the different stages of segmental glomerular hyalinosis and sclerosis with deposition of IgM and C3. At the time of renal biopsy, the serum creatinine of all except 8 patients was normal (maximally 170 mumol/1), only 13 had hypertension, and all except 2 were proteinuric. During the follow-up period (mean +/- 2Sd = 138 +/- 76 months) all of them became hypertensive. In 10 patients end-stage renal failure developed, and in another 10, serum creatinine also became elevated (range 124 - 504 mumol/1). On the basis of these data the development of focal segmental hyalinosis and sclerosis should be interpreted as a bad prognostic sign in IgA nephropathy.
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PMID:Hyperperfusion injury in IgA nephropathy. 184 42

IgA nephropathy (Berger's disease) is an important cause of end-stage renal failure in persons of Asian and European descent. We performed C4 phenotyping on plasma from 123 patients with IgA nephropathy who resided in several different parts of the United States. All of these patients underwent diagnostic renal biopsy in adulthood. Six patients had a total deficiency for the C4A protein and all six had chronic renal insufficiency (serum creatinine concentration higher than 1.4 mg/dl at last follow-up). In contrast, 47% of the patients without C4A deficiency had chronic renal insufficiency (p = 0.001). The C4 gene defect was due to deletion of both C4A genes in only two individuals, whereas three patients were heterozygous for the C4A gene deletion. We speculate that the functional alteration of the complement system related to C4A deficiency might lead to expression of clinically severe disease in an individual with a genetic susceptibility to IgA nephropathy.
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PMID:C4A deficiency and poor prognosis in patients with IgA nephropathy. 188 46

A total of 164 patients with IgA nephropathy were diagnosed at the Department of Medicine, Universiti Kebangsaan Malaysia and the Department of Nephrology, General Hospital, Kuala Lumpur between 1981-1988. This represented an incidence of 20.1% of all primary glomerulopathies seen in both units. The 3 major ethnic groups were equally affected with 59.7% occurring between the ages of 20-36 years. It was not uncommon in females. The high prevalence of hypertension, renal failure, heavy proteinuria at presentation and the increased chronicity index in the biopsy, suggest that IgA nephropathy is progressive disease leading to chronic renal failure.
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PMID:IgA nephropathy in Malaysia. 194 52

The effect of fish-oil dietary supplement on the rate of progression of renal failure in 11 patients with IgA nephropathy was investigated by comparing the slope of the plot of reciprocal serum creatinine versus time before and after supplement. After supplement, the slope significantly decreased in two patients, increased in two, and was not significantly altered in the remainder. Before supplement, serum IgA, IgA circulating immune complexes, and in-vitro Ig production were not significantly different from normal controls. After supplement, urinary protein transiently increased, serum IgA circulating immune complexes decreased, and serum triglyceride and in-vitro platelet aggregation tended to decrease. Only the change in serum IgG and spontaneous in-vitro IgG production correlated with the change in the rate of renal functional deterioration. No clinical or biochemical parameters before supplement predicted the subsequent response. In patients with IgA nephropathy, non-immune factors probably contribute to progression of renal failure, and in these patients fish-oil dietary supplement has either no demonstrable or an unpredictable effect.
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PMID:The effect of fish-oil dietary supplement on the progression of mesangial IgA glomerulonephritis. 211 20

The clinicopathological picture of 'isolated C3 mesangial nephritis' was studied in our case records. Focal and segmental or generalised deposits of C3 in the mesangium were found in 12 of 157 (7.6%) patients with primary glomerulonephritis. The clinical picture, similar to Berger's disease, was characterised by episodes of gross haematuria and/or persistent or recurrent microhaematuria and/or proteinuria. Arterial hypertension and mild renal failure were observed in one case. Light-microscopy showed minor glomerular changes such as focal and segmental increase of mesangial matrix and mesangial hyperplasia. During the short-term follow-up (median 25.5 months) no deterioration of renal function was observed. The clinical course and short-term prognosis suggest that this form of glomerulonephritis is benign.
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PMID:Clinicopathological features in patients with isolated C3 mesangial proliferative glomerulonephritis. 212 68

We report clinical and pathologic findings in 22 patients with Wegener's granulomatosis collected from 1966 to 1989. Ten cases were analyzed retrospectively. Organs affected included the lungs (n = 18), upper airways (16), kidneys (15), musculo-skeletal system (10), eyes (8), skin (7) and ear (5). Clinical manifestations of airway involvement included nasal obstruction, dysphonia and epistaxis. Lung involvement was evident in chest X-rays in 18 patients, 14 with a nodular aspects. Histologic study in 14 of these patients showed necrotizing and granulomatous vasculitis. Clinical evidence of nephropathy was evident in 15 patients and led to rapidly progressive renal failure in 8. Biopsy in this group (n = 14) revealed focal glomerulonephritis in 6 and diffuse disease in 8. Overall, 13 patients died: 5 without diagnosis, 4 from renal failure, 2 from sepsis, 1 from a lymphoma developing 3 years after immune suppressive therapy and 1 from unknown causes. Among survivors, one received a renal transplant and one remains in chronic dialysis. The diagnosis of Wegener's granulomatosis is therefore based on clinical findings including rhino pharyngeal, pulmonary and renal manifestations.
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PMID:[Wegener's granulomatosis: clinical and pathological report of 22 cases]. 213 49

We studied 78 patients with a diagnosis of IgA nephropathy. Renal biopsy was indicated in 69 patients by the presence of macroscopic hematuria (52%), microhematuria or proteinuria (22%), nephrotic syndrome (10%), severe hypertension with microhematuria or renal failure (14%) or nephritic syndrome (1%). Nine were healthy subjects being studied as live kidney donors. An association with IgG and/or IgM was present in 92% of patients. Serum IgA was elevated in 36% of patients. Hypertension was present in 30% and decreased renal function in 29%. Patients with serum creatinine above 1.5 mg/dl tended to be older (33.8 vs 28.7 years) and to have hypertension (52% vs 19%). Among 25 patients followed for more than 12 months renal function remained stable in 44%, deteriorated in 20% and 36% developed renal failure. The latter was associated to older age, hypertension, absence of macroscopic hematuria and nephrotic syndrome. The 9 live donors had no clinical manifestations of renal disease. Thus, IgA nephropathy is a highly variable clinical entity, both in its manifestations and its prognosis. An asymptomatic course is demonstrated in some subjects.
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PMID:[IgA nephropathy (Berger's disease). Our experience in 78 cases]. 215 41

We have studied 209 patients with IgA nephropathy. 26 were hypertensive at the time of renal biopsy, and 59 patients developed hypertension during follow-up. Survival statistics show that only 45% of the patients will remain normotensive 10 years after renal biopsy. The presence of hypertension at renal biopsy correlated well with the usual parameters of a poor prognosis. The same markers predicted a later development of hypertension in patients who were normotensive at the time of renal biopsy. When hypertension is established, the prognosis is poor. Three years after diagnosis of hypertension, the renal survival was found to be 70% in the 59 patients we have followed. It is also possible that the markers of a poor prognosis actually predict the progression rate rather than the prognosis, because in time, some patients with initially mild manifestations of the disease will progress to end-stage renal failure.
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PMID:Development of hypertension in IgA nephropathy as a marker of a poor prognosis. 224 56

The association of HBV infection and glomerular damage was first reported by Combes et al in 1971, in a patient with nephrotic syndrome due to membranous glomerulopathy and chronic hepatitis B. Since, then, other glomerular diseases have been reported such as a) minimal changes nephropathy, b) IgA nephropathy, c) membranous-proliferative glomerulonephritis (MPGN), d) membranous, e) mesangial proliferative and f) lupus nephritis. All of them are associated with chronic hepatic disease and some of the following antigens: 1) HBsAg; 2) HBeAg; 3) HBcAg. These disorders are very frequent in Southeast Asia. Vertical transmission from mothers to fetuses may be important in maintaining the high carrier rate, and possibly plays a role in the development of glomerular damage. On the other hand, MPGN associated with HBsAg has rarely been reported and always with a favorable benign course. The present report describes interesting findings in a renal biopsy from a HBsAg and HBeAg carrier, who developed renal failure requiring hemodialysis. A 21 year old Korean man was admitted to the Hospital for nephrotic syndrome, microhematuria hypertension and renal failure. He had no previous history of blood transfusion, intravenous drug addiction, jaundice or liver disease. His father was HBsAg carrier with hepatic cirrhosis. An ultrasound examination showed normal renal size. Renal biopsy was performed and the patient received hemodialysis treatment. The specimen was processed for light microscopy, immunofluorescent studies and peroxidase-antiperoxidase technique. Frozen sections were studied by direct immunofluorescence for the identification of IgG, IgA, C1q, C3, fibrinogen and albumin. Paraffin sections stained by immunoperoxidase technique for HBsAg, using polyclonal monospecific rabbit anti-Human antisera (Dakopatts, Copenhagen).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Membranoproliferative glomerulonephritis with semilunar forms and massive deposits of IgA associated with HBsAg]. 229 14


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